Haematology & Immunology Flashcards
What are the main features of myeloma? (CRAB)
→ HyperCalcaemia
→ Renal failure
→ Anaemia
→ Bone disease
What is lactate a marker of?
Is a high or low lactate good?
Hypoperfusion (reduced O2 reaching the tissues)
LOW lactate - the higher the lactate, the more tissues are without O2!
What is the function of haptoglobin?
It transports free haemoglobin in the bood → reticuloendothelial system to be recycled
Which ethnic group is sepsis most common within?
Asians
What is a characteristic finding on a blood film that indicates Hodgkins lymphoma?
Reed-sternberg cells
List 4 risk factors for Hodkins lymphoma:
What is the key presenting symptom?
What is the diagnostic test/ investigation?
~ What is a key finding in this?
What is the staging used in all lymphoma’s? - describe the stages
→ Smoking
→ Epstein barr virus
→ HIV
→ Immunosuppression
Lymphadenopathy - non-tender, alcohol causes pain in lymph nodes
Lymph node biopsy
~ Reed sternberg cells
Ann Arbor Staging:
Stage 1: Only 1 lymph node group affected
Stage 2: Several lymph nodes affected but on the same side of diaphragm
Stage 3: Several lymph nodes affected but on different sides of diaphragm
Stage 4: Organ invovlement (eg, lungs/ liver)
What is the name given for premature RBCs? (these are the RBCs just before they are released into the circulaton)
Reticulocytes
What is the difference between petechiae & purpura?
What is ecchymoses?
- *Petechiae** < 3mm
- *Purpura** 4 - 10mm
Ecchymoses is bleeding under the skin that is larger than 1cm!
In haemotology, what is the function of G6PD?
What is the result of a G6PD deficiency?
List some common triggers of this: (3)
What ar the common clinical features seen? (3)
G6PD is an enzyme that attaches onto RBCs to protect them against oxidative stress
G6PD deficiency causes haemolysis of RBC when there is oxidative stress → haemolytic anaemia
1) Infection
2) Broad beans (fava beans)
3) Drugs (antimalarials, nitrofurantoin, aspirin)
1) Anaemia
2) Jaundice
3) Splenomegaly
Anaphylaxis is what type of hypersensitivity reaction?
This type of reaction is mediated by what?
Type 1 hypersensitivity reaction
IgE mediated mast cell degranulation
What is Immune Thrombocytopenic Purpura (ITP)?
What blood abnormality does it result in?
What is the 1st line treatment for ITP?
If this doesn’t work, what do you add to the treatment?
Autoimmune attack of platelets (antibodies are made against platelets)
Results in thrombocytopenia (low platelet count)
1st line treatment: steroids
If steroids don’t work, add in IV IgG (immunoglobulins)
What blood levels of Hb would indicate anaemia in:
- a -* females
- b -* males
Females: < 120 g/L
Males: < 140 g/L
What is a characteristic finding on a blood film that indicates acute myeloid leukamia?
Auer rods
What system is used to stage lymphoma’s?
Ann Arbor staging
Cancers within the bone marrow can cause what result on a FBC?
Why can this occur?
Pancytopenia
Occurs when the cancerous occupy most of the space within the bone marrow - normal blood cells are unable to develop!
Give the medical name for a red blood cell.
What is the name given to the production of RBCs?
What hormone is responsible for stimulation of RBC production?
Where is this hormone secreted from & why is it secreted?
Erythrocyte
Erythropoesis
Erythropoietin
Kidney in response to hypoxia
What are the 2 antibiotics that are started if neutropenic sepsis is suspected?
~ Tazocin
~ Gentamicin
What immunological mechanism is responsible for type 2 hypersensitivity reactions?
Auto-antibody mediated receptor activation
What is the qSOFA score used for?
What 3 variables does the qSOFA consider?
A score of what suggests a poor prognosis?
Used on patients with a suspected/ confirmed infection to predict the patients who would likely require a higher level of care & have a poorer prognosis
→ BP
→ Mental state (level of conscousness)
→ Respiratory rate
Score of 2 or more
What is the prophylaxis management of haemophilia?
How is an acute episode of bleeding treated? (3)
Replacement of clotting factors via IV transfusions (VIII - A, IX - B)
1) Infusions of affected clotting factor (VIII or IX)
2) Desmopressin (DDAVP) - to stimulate VWF release
3) Tranexamic acid - reduces the rate of fibrinolysis so that clot remains for longer
List some causes for a decreased production of RBC’s in the bone marrow (4)
Bone marrow disorder
Chronic kidney disease (reduced secretion of erthyropoietin reduces RBC production!)
Hypothyroidism (thyroid hormones also stimulate RBC production)
Iron & vitamin B12 deficiency (these are needed for functional RBC production)
What is the abnormality that results in polycythaemia vera?
What mutation is associated with polycythaemia vera?
List some clinical signs/ symptoms of this condition: (5)
What is the management of this condition?
Proliferation of RBC’s
JAK2 mutation
- Red face (plethora)
- Vascular occlusion (DVT/ PE/ Stroke)
- Splenomegaly
- Headaches
- Itchy, especially after hot bath
Management: venesection (to prevent hyperviscosity of blood) & aspirin
Name the 2 divisions of the immune system:
Innate & adaptive immune systems
Regarding fluids, (colloid & crystalloid’s):
1) give an example of each type commonly used in hospital
2) describe the size of the molecules they contain & the consequence of this on fluid compartments within the body
3) state a contraindiction in each type
- *1) Colloid**: fluid containing starch/ gelatin
- *Crystalloid**: plasmalyte/ hartmans/ dextrose/ 0.9%NaCl
- *2) Colloid:** large molecules → more fluid is retained in the blood vessels
- *Crystalloid:** small molecules → some fluid remains in blood vessels & some moves into the tissues/ cells
- *3)** Colloid: the large molecules can cause kidney damage (so cannot be used in patients with renal failure)
- *Crystalloid:** 0.9%NaCl has a high Na conc so can cause hypernatraemia
What is lactate a marker of?
Is a high or low lactate good?
Hypoperfusion (reduced O2 reaching the tissues)
LOW lactate - the higher the lactate, the more tissues are without O2!
What abnormality is seen in haemophilia A?
What abnormality is seen in haemophilia B?
What is the mode of inheritance of haemophilia?
What tests would you do to diagnose haemophilia and what results would you expect in haemophilia? (3)
Haemophilia A: deficiency of clotting factor VIII
Haemophilia B: deficiency of clotting factor IX
X linked recessive
1) Clotting factor tests - to look at levels of factors VIII & IX (low VIII in haemophila A & low IX in haemophilia B)
2) Blood test- APTT*: prolonged
3) Blood test- prothrombin: normal
* APTT = blood test that measures time taken for blood to clot
Which electrolyte abnormality can blood transfusions cause?
Why does this happen?
Hypocalcaemia
When blood is donated, it’s mixed with sodium citrate to prevent it from coagulating. → The citrate in the blood can bind to the patient’s circulating calcium resulting in a decreased amount of free calcium = symptoms of hypocalcaemia
What test would be used to test for an autoimmune cause of haemolytic anaemia?
What result would suggest an autoimmune cause & what would be seen in the lab?
DAT test (direct antiglobulin test) / coombs test (old name)
Positive result = immune mediated
Agglutination of RBCs (they clunp together)
List some common presentations of von Willebrand disease: (5)
→ nose bleeds
→ menorrhagia
→ bleeding gums when brushing teeth
→ prolonged, heavy bleeding during surgery/ trauma
→ easy bruising
What is the normal range of WBC in blood?
4 - 10 x109/L
What are 3 commonest pathogens responsible for causing neonatal sepsis?
What antibiotics are used in the 1st line management of neonatal sepsis?
1) Group-B strep
2) E.Coli
3) Listeria
IV penicillin & gentamicin
What is the function of Von Willebrand Factor?
What abnormality results in von Willebrand disease?
What is the mode of inheritance of VWD?
VWF is vital for clot formation: • links platelets to the exposed, damaged vessel wall • stabilises factor VIII so that it can work for longer
A deficiency of, or dysfunctional VWF
Autosomal dominant
What is the treatment of von Willebrand disease?
List 2 contraindictations to the use of DDAVP:
There is no day-to-day treatment. Treatment is given after a bleed or in preparation for surgery
1) VWF concentrate IV
2) Desmopressin - stimulates the release of VWF
3) Tranexamic acid - inhibits fibrinolysis (clot breakdown)
Contraindictations: young children, people with high cardiovascular risk
What is an autologous transplant?
What is an allogeneic transplant?
What is a syngeneic transplant?
What is an xenogeneic transplant?
What type of transplant has the highest risk of rejection?
Autologous transplant: tissue from the same person
Allogeneic transplant: tissue from another member of the same species (eg, human - human)
Syngeneic transplant: tissue from an identical twin
Xenogeneic transplant: tissue from a different species
Xeogeneic transplant has the biggest risk of rejection as it is tissue from another species
What is the cellular pathology that results in pernicious anaemia?
Autoimmune attack against intrinsic factor → B12 cannot be absorbed without intrinsic factor and patient becomes anaemic
What is a characteristic finding on a blood film that indicates chronic lymphocytic leukaemia?
Smudge cells
Skin prick testing is used to test for what type of hypersensitivity reaction?
Patch testing is used to test for what type of hypersensitivity reaction?
Skin prick testing = hypersensitivity I
Patch testing = hypersensitivity IV
What is the function of haptoglobins?
They remove free haemoglobin from the circulation
What chromosome is associated with chronic myeloid leukaemia? - what are the consequences of this?
What is the gene translocation?
What is the 1st line management of CML?
Philadelphia chromosome ⇒ BCR-ABL gene (oncogene)
t (9;22)
Tyrosine kinase inhibitors (inhibit BCR-ABL!)
~ eg Imatinib
What is the difference between Hodgkins and Non-Hodgkins lymphoma?
Hodgkins lymphoma is characterised by the presence of Reed-Sternberg cells → Non-Hodgkins lymphoma does not have these cells.
* Reed-Sternberg cells are abnormally large lymphocytes that usually have multiple nuclei
What immunological mechanism is responsible for type 2 hypersensitivity reactions?
Give 2 examples of conditions that this occurs in:
Auto-antibody mediated receptor activation
Haemolytic disease of the newborn
Transfusion reactions
You are working in A&E and a patient is hypotensive. What do you do to increase the BP?
How much of this would you give and over what time?
IV fluid resuscitation
500ml saline or plasmalyte bolus over 15 mins
What is a type 4 hypersensitivity reaction?
Give 2 examples of conditions that are caused by type 4 hypersensitivity reactions:
Delayed hypersensitivity reaction, mediated by T cells
Autoimmune conditions:
Rheumatoid arthritis
Type 1 Diabetes
What are the cancerous cells in myeloma & what do they produce? - explain what these are..
List some signs/ symptoms of myeloma: (4)
Name the definitive investigation of myeloma:
What would be seen on a bone marrow biopsy? - state what would qualify as myeloma
Plasma cells - produce paraproteins
Paraproteins = identical immunoglobulins (usually IgG) produced by a (cancerous) clonal population of plasma cells
- Hypercalcaemia
- Renal failure
- Anaemia
- Lytic bone disease/ pain
Serum protein electrophoresis
Bone marrow biopsy: high plasma cells
~ plasma cells >10% = myeloma
~ plasma cells 3-10% = MGUS
What is graft vs host disease?
How can the risk of GVHD be minimised?
Rejection of a transplant caused by the donor’s T cells attacking the recipant’s antigens !!
Immunosuppression!
• steroids
• cyclosporin/ rapamycin
In haematology, what 3 things are considered as ‘B symptoms’?
Night sweats, weight loss, fever
What is the commonest blood cancer of children?
What blood cell line does this cancer arise from?
List some symptoms/ signs of this cancer: (4)
What is the definitive investigation? What will be seen on this?
What is the treatment of this cancer?
Acute lymphoblastic leukaemia
Lymphoid progenitor cells (undifferentiated)
- Child with a limp
- Bone/ joint pain
- Exertional SOB
- Pancytopenia
Bone marrow biopsy - blast cells
Prolonged course of chemotherapy
What cells are cancerous in acute myeloid leukaemia? - where in the body are these cancerous cells found? (before mets)
List some clinical signs/ symptoms of AML: (4)
What is the definitive investigation of AML?
~ List 2 things that would be seen on this
What is the treatment of AML?
Undifferentiated, myeloid progenitor cells
~ found in the bone marrow
- Pancytopenia
- Gum hypertrophy
- Hepatosplenomegaly
- Petechiae & abnormal bleeding (caused by low platelets)
Bone marrow biopsy
• > 20% blast cells
• auer rods
Chemotherapy +/- stem cell transplant
Name the 2 types of lymphocytes and name where they each mature
T cells - thymus
B cells - bone marrow
Why does physiological anaemia occur during pregnancy?
Blood volume increases during pregnancy, but plasma volume > RBC = anaemia (as RBC’s are diluted!)
Which compound is released from damaged vessel walls and initiates the coagulation cascade?
Tissue factor
What does SIRS stand for?
What clinical features would a patient have, to be diagnosed with SIRS?
Systemic inflammatory response syndrome
→ High/low temperature
→ HR > 90
→ RR > 20
→ High CO2
→ High WBC’s
Give examples of conditions that cause a normocytic anaemia: (4)
What initial investigation would you do after identifying normocytic anaemia & what would high / low results suggest?
1) Blood loss
2) Haemolysis of RBC (aka, haemolytic anaemia)
3) Bone marrow disease (failure/ cancer infiltration)
4) Secondary anaemia (eg, inflammation)
Reticulocyte count:
High reticulocyte = Blood loss, haemolysis
Low reticulocyte = Bone marrow disease, secondary anaemia
What is the medical word for a high platelet count?
What is the medical word for a low platelet count?
Thrombocytosis
Thrombocytopenia
What immunological mechanism is responsible for type 3 hypersensitivity reactions?
Give an example of a disease that is caused by type 3 hypersensitivity.
Immune complex deposition
SLE
What are the main features of myeloma? (CRAB)
→ HyperCalcaemia
→ Renal failure
→ Anaemia
→ Bone disease
What does SCID stand for?
Which immune cells are affected in SCID?
What are the 2 treatment options for SCID?
Severe combined immunodeficiency
Development of B cells & T cells is affected producing dysfunctional B & T cells
1st line = stem cell transplant
If not available: gene therapy
List some common symptoms of anaemia: (5)
→ Fatigue
→ SOB
→ Headaches
→ Pre-syncope / syncope
→ Palpitations
What is the prophylaxis management of haemophilia?
How is an acute episode of bleeding treated? (3)
Replacement of clotting factors via IV transfusions (VIII - A, IX - B)
1) Infusions of affected clotting factor (VIII or IX)
2) Desmopressin (DDAVP) - to stimulate VWF release
3) Tranexamic acid - reduces the rate of fibrinolysis so that clot remains for longer
Name the 3 hormones that stimulate RBC production in the bone marrow:
Erythropoietin
Thyroid hormone
Androgens
List some clinical features seen in haemophilia: (5)
Haemarthrosis (bleeding into the joints)
Muscle haematoma
CNS bleeding
Prolonged bleeding after surgery/ trauma
Menorrhagia
The Philadelphia chromosome is associated with what haematological condition?
The philadelphia chromosome (a mix of 2 chromosomes) results in what oncogenic gene?
Chronic myeloid leukaemia
BCR-ABL gene
What type of anaemia does sickle cell disease cause?
Would you expect a high or low reticulocyte count? - why?
Normocytic anaemia (normal MCV (RBC size))
Raised reticulocyte count
~ there is increased haemolysis of RBC and thus the bone marrow chucks out more reticulocytes to try to compensate in the loss of RBC (although it doesn’t work as reticulocytes are immature RBC!)
There are 3 types of von Willebrand Disease, describe the problem associated with each type:
Which type(s) presents with the most severe symptoms?
Type 1: there isn’t enough VWF in the body
Type 2: there is enough VWF, however it is dysfunctional
Type 3: almost complete deficiency of VWF
Types 2 & 3 are more severe
What cells are cancerous in myeloproliferative disorders? - where in the body are these cancerous cells found? (before mets)
List some clinical signs/ symptoms of chronic myeloid leukaemia (a myeloproliferative disorder) (4) - what is the cancerous cell?
What chromosome is associated with CML? - what are the consequences of this?
What is the 1st line management of CML?
Differentiated cells of myeloid origin
~ found in bone marrow
• Anaemia (→ pancytopenia)
• Massive splenomegaly
• HIGH WCC
• Gout
~ Cancerous cell = neutrophils
Philadelphia chromosome ⇒ BCR-ABL gene (oncogene)
Tyrosine kinase inhibitors (inhibit BCR-ABL!)
What are the 6 components of sepsis 6?
~ state the order you would do these in
(take 3, give 3)
1) Give O2 if sats are below 94%
2) Take blood cultures
3) Give IV antibiotics
4) Fluid challenge (give IV fluids)
5) Measure blood lactate
6) Measure urine output
What are the 6 components of sepsis 6?
~ state the order you would do these in
(take 3, give 3)
1) Give O2 if sats are below 94%
2) Take blood cultures
3) Give IV antibiotics
4) Fluid challenge (give IV fluids)
5) Measure blood lactate
6) Measure urine output
What does thrombocytopenia mean?
List some common presentations of thrombocytopenia: (5)
Low platelet count
→ Petechiae
→ Ecchymosis (bruising)
→ Nose bleeds
→ Bleeding gums
→ Menorrhagia
What condition is indicated if a woman presents with recurrent miscarriages & a history of VTE events?
What is the treatment of this condition? (2)
Antiphospholipid syndrome
Aspirin & LMWH
SIRS + infection = ?
What is the condition called if a patient has end organ damage as a result of sepsis?
What is the difference between severe sepsis & septic shock?
Sepsis
Severe sepsis
In septic shock, the patient has hypotension as well as severe sepsis
A 16y boy presents with central abdominal pain & haematuria for 1 week. He also complains of pain in both knees. Examination reveals a non-blanching purpuric rash on his legs & buttocks. Urine dip shows blood ++ & protein +, kidney function is abnormal.
What is the most likely diagnosis? - what is this?
List the 4 common presenting features of this condition:
What is the management of this condition?
What monitoring needs to be done? (2)
Henoch-Schonlein Purpura - A type of IgA vasculitis
- Purpura (rash on legs → buttocks)
- Joint pain (commonly knee’s & ankles)
- Abdominal pain
- Renal impairment
Management: supportive (analgesia, rest, hydration)
~ most usually resolve within 4-6 weeks.
Monitoring: needed whilst the disease is still active:
• urine dipstick (to monitor renal impairment)
• blood pressure (to monitor for hypertension)
What is a characteristic finding on a blood film that indicates multiple myeloma?
Rouleaux formation
List some causes of intravascular haemolysis: (3)
List some causes of extravascular haemolysis: (4)
Intravascular:
→ Mechanical heart valve
→ Acute transfusion reaction (if blood transfused is mis-matched)
→ Infections, eg malaria
→ G6PD deficiency
→ Autoimmune haemolytic anaemia
Extravascular:
→ Hypersplenism (spleen works harder than normal)
→ Haemoglobinopathys (eg thalassaemia, sickle cell)
Name the 2 ways that anaemia can be categorised by:
- Looking at the mean corpuscular volume (MCV) of the RBCs
- The mechanism of cause of anaemia
(RBC size!)
What genetic mode of inheritance is seen in haemophilia A & B?
Which sex is haemophilia more common in?
X linked recessive inheritance!
Males
What does SCID stand for?
Which immune cells are affected in SCID?
What are the 2 treatment options for SCID?
Severe combined immunodeficiency
Development of B cells & T cells is affected producing dysfunctional B & T cells
1st line = stem cell transplant
If not available: gene therapy
In a centrifuge, what 3 components will blood separate into?
Name some cells that will be found in each component.
Plasma
→ Clotting factors
→ Albumin (& other proteins)
→ Antibodies
Buffy coat
→ Platelets
→ WBC’s (leucocytes)
Red blood cells
What are hypersensitivity reactions?
Exaggerated immune responses that cause damage to tissues/ blood
If a woman is *Rh- and is carrying a Rh+ baby and there is no intervention, what will happen during delivery/ when there is mixing of blood?
Why does this happen?
When should this be checked for during pregnancy?
What can be given as prophylaxis for this?
*Rh = rhesus
The women will start developing anti-D antibodies after any sensitising event (commonly giving birth)
If someone is rhesus negative, they don’t have the D antigen on their RBC’s so if their blood comes into contact with someone that is rhesus positive then their blood will start producing antibodies against the foreign antigens.
Rh status of mother & baby is checked at the booking appointment (week 10)
If mother is negative & baby is positive, prophylaxis = anti D injection at 28 weeks gestation PLUS immediately after any sensitising events
What is the definition of sepsis?
Life threatening organ dysfunction caused by a dysregulated host response to an infection
What is the treatment of von Willebrand disease?
List 2 contraindictations to the use of DDAVP:
- There is no day-to-day treatment. Treatment is given after a bleed or in preparation for surgery*
1) VWF concentrate IV
2) Desmopressin - stimulates the release of VWF
3) Tranexamic acid - inhibits fibrinolysis (clot breakdown)
Contraindictations: youung children, people with high cardiovascular risk
When looking at the mean corpuscular volume of RBCs (size), what are the 3 types that may be seen?
Microcytic anaemia (small size)
Normocytic anaemia (normal size)
Macrocytic anaemia (large size)
If a woman is *Rh- and is carrying a Rh+ baby and there is no intervention, what will happen during delivery/ when there is mixing of blood?
Why does this happen?
When should this be checked for during pregnancy?
What can be given as prophylaxis for this?
*Rh = rhesus
The women will start developing anti-D antibodies after any sensitising event (commonly giving birth)
If someone is rhesus negative, they don’t have the D antigen on their RBC’s so if their blood comes into contact with someone that is rhesus positive then their blood will start producing antibodies against the foreign antigens.
Rh status of mother & baby is checked at the booking appointment (week 10)
If mother is negative & baby is positive, prophylaxis = anti D injection at 28 weeks gestation PLUS immediately after any sensitising events
There are 2 types of immunity: innate & adaptive:
1) Which one is activated in a primary/ secondary infection?
2) Which one is rapid & non-specific/ slow onset & very specific?
3) Which one provides ‘short’/ ‘long’ term immunity?
4) Which one involves phagocytes & the complement system?
5) Which one invovles antibodies and cellular immunity (provided by T cells)?
1) Primary infection = innate
* *Secondary** infection = adaptive
2) Rapid & non specific = innate
* *Slow & very specific** = adaptive
3) Short term immunity = innate
* *Long term immunity** = adaptive
4) Phagocytes & complement = innate
5) Antibody production & cellular immunity = adaptive
What is the normal range of haemoglobin in:
- Males
- Females
Males: 140 - 180 g/L
Females: 120 - 160 g/L
Ferroportin is vital for what?
What compound blocks the action of ferroportin & what is the consequence of this?
Which organ produces this compound and in response to what 2 things?
Ferroportin is vital for iron absorption from gut & iron storage in cells, mainly liver
Hepcidin blocks ferroportin preventing further iron absorption
Liver produces hepcidin in response to:
1) high iron stores (when they are full and the body doesn’t need any more iron)
2) inflammation
List some common signs of anaemia: (4)
→ Pallor of skin
→ Pallor of conjunctiva
→ Tachycardia
→ Raised respiratory rate
What is the average lifespan of a RBC?
How are RBCs removed from the circulation?
Which 2 organs are involved in this process?
120 days
The reticuloendothelial system removes RBCs from the circulation
Spleen & liver
What is the normal range of platelets in blood?
150 - 400 x109/L
What are the cancerous cells in chronic lymphocytic leukaemia?
List some symptoms/ signs of CLL: (4)
What autoimmune condition is associated with CLL?
What cell would be seen on a blood film?
What is the management of CLL? - is it curable?
Differentiated lymphoid cells (B & T lypmhocytes)
- COMMONLY ASYMPTOMATIC !!!!
- Non-tender lymphadenopathy
- Hepatosplenomegaly
- B symptoms
Warm autoimmune haemolytic anaemia
Smudge cells
NOT CURABLE - if no symptoms, don’t treat!
(Otherwise chemotherapy)
There are 5 acute and 1 delayed complications associated with blood transfusions. Name each of these and describe the presentation/clinical features of each one:
Anaphylactic/ allergic transfusion reaction:
~ urticaria/ angioedema/ wheeze
~ hypotension
Acute haemolytic transfusion reaction:
ABO incompatibility
~ fever
~ hypotension
~ anxiety
~ DIC
~ jaundice
Transfusion related acute lung injury:
~ pulmonary oedema
~ SOB, increased RR
~ hypotension
Transfusion associated circulatory overload:
~ fluid overload (pulmonary oedema/ ankle oedema)
~ hypertension
Febrile non-haemolytic transfusion reaction:
~ fever +/- rigors/chills
*** patients are otherwise completley FINE ***
Delayed haemolytic transfusion reaction:
Rhesus incompatibility - usually 5 days AFTER transfusion
~ jaundice
~ anaemia
~ fever
A 35y/o man has been recently diagnosed with Hodgkin’s lymphoma. He started the first day of his chemotherapy yesterday, but since then has not been feeling well. The FY2 on the ward checked his U&E and found some abnormalities including hyperkalaemia, hyperphosphataemia and hypocalcaemia.
What is the likely complication that this man has suffered from?
What can be given as prophylaxis against this complication?
Tumour lysis syndrome
Allopurinol
A patient had their first chemotherapy yesterday for an acute leukaemia and today they state that they’re not feeling very well. This morning’s bloods show renal impairment and a high uric acid.
What is the likely diagnosis?
Why does this happen?
Which electrolyte abnormalities would you expect to see?
Tumour lysis syndrome
TLS occurs due to rapid breakdown of tumour cells and thus release of intracellular contents into the blood (especially uric acid)
- HIGH potassium
- HIGH phosphate
- LOW calcium
Name the commonest leukaemia in children:
Which genetic condition does this leukaemia affect the most?
Acute lymphoblastic leukaemia
Downs syndrome
Name the leukaemia that can transform into a high grade lymphoma:
What is this transformation called?
What diagnostic cells would you see on a blood film in this leukaemia?
Chronic lymphocytic leukaemia
Richter’s transformation
Smudge / smear cells
Which blood cancer is associated with the Philadelphia chromosome?
What is the translocation of this chromosome?
Chronic myeloid leukaemia
t(9:22)
Which leukaemia is often the result of the transformation of a myeloproliferative disorder?
What diagnostic cells would you see on a blood film in this leukaemia?
Acute myeloid leukaemia
Auer rods
Which 2 blood cancers would you expect to see blast cells in?
ACUTE myeloid leukaemia
ACUTE lymphoblastic leukaemia
